Hearing loss from intense noise exposure and ototoxic drugs greatly reduces the neural output of the cochlea. Despite a reduced cochlear output, neural activity in the central auditory pathway often becomes hyperactive at suprathreshold intensities indicative of Enhanced Central Gain. Enhanced Central Gain is believed to be responsible for hyperacusis, a condition in which listeners experience everyday sounds as unbearably loud or even painful. The goals of this project are: (1) Determine if Enhanced Central Gain is responsible for the temporal and spectral features of hyperacusis, (2) Determine how the acoustic environment (sound enrichment/deprivation) modulates hyperacusis/loudness growth and Central Gain and (3) Determine how serotonin and GABA agonists/antagonists affect hyperacusis and Central Gain. The proposed studies will increase our understanding of the neural mechanisms of hyperacusis and test the efficacy of pharmacological agents to treat hyperacusis.